Heart failure is a debilitating disease in which abnormal function of the heart leads in the direction of inadequate blood flow to fulfill the needs of the tissues and organs of the body. Typically, the heart loses propulsive power because the cardiac muscle loses capacity to stretch and contract. Often, the ventricles do not adequately eject or fill with blood between heartbeats and the valves regulating blood flow become leaky, allowing regurgitation or back-flow of blood. The impairment of arterial circulation deprives vital organs of oxygen and nutrients. Fatigue, weakness and the inability to carry out daily tasks may result. Not all heart failure patients suffer debilitating symptoms immediately. Some may live actively for years. Yet, with few exceptions, the disease is relentlessly progressive. As heart failure progresses, it tends to become increasingly difficult to manage. Even the compensatory responses it triggers in the body may themselves eventually complicate the clinical prognosis. For example, when the heart attempts to compensate for reduced cardiac output, it adds muscle causing the ventricles (particularly the left ventricle) to grow in volume in an attempt to pump more blood with each heartbeat. This places a still higher demand on the heart's oxygen supply. If the oxygen supply falls short of the growing demand, as it often does, further injury to the heart may result. The additional muscle mass may also stiffen the heart walls to hamper rather than assist in providing cardiac output. A particularly severe form of heart failure is congestive heart failure (CHF) wherein the weak pumping of the heart leads to build-up of fluids in the lungs and other organs and tissues.
Heart failure has been classified by the New York Heart Association (NYHA) into four classes of progressively worsening symptoms and diminished exercise capacity. Class I corresponds to no limitation wherein ordinary physical activity does not cause undue fatigue, shortness of breath, or palpitation. Class II corresponds to slight limitation of physical activity wherein such patients are comfortable at rest, but wherein ordinary physical activity results in fatigue, shortness of breath, palpitations or angina. Class III corresponds to a marked limitation of physical activity wherein, although patients are comfortable at rest, even less than ordinary activity will lead to symptoms. Class IV corresponds to inability to carry on any physical activity without discomfort, wherein symptoms of heart failure are present even at rest and where increased discomfort is experienced with any physical activity.
The current standard treatment for heart failure is typically centered on medical treatment using angiotensin converting enzyme (ACE) inhibitors, diuretics, beta-blockade, and digitalis. Cardiac resynchronization therapy (CRT) may also be employed, if a bi-ventricular pacing device is implanted. Briefly, CRT seeks to normalize asynchronous cardiac electrical activation and resultant asynchronous contractions associated with CHF by delivering synchronized pacing stimulus to both ventricles. The stimulus is synchronized so as to improve overall cardiac function. This may have the additional beneficial effect of reducing the susceptibility to life-threatening tachyarrhythmias. CRT and related therapies are discussed in, for example, U.S. Pat. No. 6,643,546 to Mathis et al., entitled “Multi-Electrode Apparatus and Method for Treatment of Congestive Heart Failure”; U.S. Pat. No. 6,628,988 to Kramer et al., entitled “Apparatus and Method for Reversal of Myocardial Remodeling with Electrical Stimulation”; and U.S. Pat. No. 6,512,952 to Stahmann et al., entitled “Method and Apparatus for Maintaining Synchronized Pacing.”
Pulmonary edema is a swelling and/or fluid accumulation in the lungs often caused by heart failure (i.e. the edema represents one of the “congestives” of CHF.) Briefly, the poor cardiac function resulting from heart failure can cause blood to back up in the lungs, thereby increasing blood pressure in the lungs. The increased pressure pushes fluid—but not blood cells—out of the blood vessels and into lung tissue and air sacs. This can cause severe respiratory problems and, left untreated, can be fatal. Pulmonary edema is usually associated with relatively severe forms of heart failure and is often asymptomatic until the edema itself becomes severe, i.e. the patient is unaware of the pulmonary edema until it has progressed to a near fatal state when respiration suddenly becomes quite difficult.
In view of the potential severity of heart failure/pulmonary edema, it is highly desirable to detect the onset of these conditions within a patient and to track the progression thereof so that appropriate therapy can be provided. Many patients suffering heart failure/pulmonary edema already have pacemakers or ICDs implanted therein or are candidates for such devices. Accordingly, it is desirable to provide such devices with the capability to automatically detect and track heart failure/pulmonary edema.
Heretofore, a number of techniques have been developed for detecting heart failure and/or pulmonary edema using implantable cardiac devices based on analysis of a thoracic impedance signal. See, for example, U.S. Pat. No. 5,876,353 to Riff, entitled “Impedance Monitor for Discerning Edema through Evaluation of Respiratory Rate”; U.S. Pat. No. 5,957,861 to Combs et al., entitled “Impedance Monitor for Discerning Edema through Evaluation of Respiratory Rate”; U.S. Pat. No. 6,512,949 also to Combs et al., entitled “Implantable Medical Device for Measuring Time Varying Physiologic Conditions Especially Edema and for Responding Thereto”; U.S. Pat. No. 6,473,640 to Erlebacher, entitled “Implantable Medical Device for Measuring Time Varying Physiologic Conditions Especially Edema and for Responding Thereto”; U.S. Pat. No. 6,595,927 to Pitts-Crick et al., entitled “Method and System for Diagnosing and Administering Therapy of Pulmonary Congestion”; U.S. Pat. No. 6,829,503 to Aft, entitled “Congestive Heart Failure Monitor”; and U.S. Patent Application 2004/0102712 of Belalcazar et al., entitled “Impedance Monitoring for Detecting Pulmonary Edema and Thoracic Congestion.”
However, it would be desirable to provide improved techniques, particularly for detecting pulmonary edema, via thoracic impedance and is to this end that aspects of the invention are directed. In this regard, previous techniques for detecting pulmonary edema based on impedance are often unduly complex. In some cases, changes in impedance due to other factors besides the fluids associated with pulmonary edema can possibly result in a false positive detection of pulmonary edema.
Many patients with heart failure and/or pulmonary edema also suffer from episodes of reduced respiration, such as apnea or hypopnea. With hypopnea, respiration is reduced but is still present. With apnea, however, respiration may cease completely for a minute or longer. One common form of apnea is sleep apnea, in which episodes can occur hundreds of times during a single night. Accordingly, patients with sleep apnea experience periodic wakefulness at night and excessive sleepiness during the day. In addition, apnea can exacerbate various medical conditions, particularly CHF.
One form of apnea is central sleep apnea (CSA), which is believed to be the result of a neurological condition. Briefly, respiration is regulated by groups of nerve cells in the brain in response to changing blood chemistry levels, particularly blood CO2 levels. When blood CO2 levels exceed a certain threshold, the groups of nerve cells generate a burst of nerve signals for triggering inspiration. The inspiration nerve signals are relayed via phrenic nerves to the diaphragm and via other nerves to chest wall muscles, which collectively contract to expand the lungs. With CSA, the nerve signals are not properly generated during extended periods of time while the patient is asleep or are of insufficient magnitude to trigger sufficient muscle contraction to achieve inhalation. In either case, the patient thereby fails to inhale until appropriate inspiration nerve signals are eventually generated—often not until after the patient awakes in response to significantly high blood CO2 levels. Arousal from sleep due to CSA usually lasts only a few seconds, but such brief arousals nevertheless disrupt continuous sleep and can prevent the patient from achieving rapid eye movement (REM) sleep, which is needed. In addition, as already noted, frequent periods of apnea can exacerbate other medical conditions. In particular, aberrant blood chemistry levels occurring by sleep apnea are a significant problem for patients with CHF. Due to poor cardiac function caused by CHF, patients already suffer from generally low blood oxygen levels. Frequent periods of sleep apnea result in even lower blood oxygen levels. Fortunately, CSA is rare.
Another form of apnea, which is more common, is obstructive sleep apnea (OSA) wherein the respiration airway is temporarily blocked. With OSA, proper inspiration nerve signals are generated by the brain and so the diaphragm and chest muscles contract in an attempt to cause the lungs to inhale. However, an obstruction of the respiration airway blocks delivery of air to the lungs and so blood CO2 levels continue to increase, usually until the patient awakens and readjusts his or her position so as to reopen the obstructed respiration pathway so that normal breathing can resume. The site of obstruction is usually the soft palate, near the base of the tongue, which lacks rigid structures such as bone or cartilage for keeping the airway open. While the patient is awake, muscles near the soft palate keep the passage open. However, while asleep, the muscles can relax to a point where the airway collapses and hence becomes obstructed. As with CSA, arousal from sleep usually lasts only a few seconds but is sufficient to disrupt continuous sleep and prevent proper REM sleep. It is estimated that OSA occurs in approximately two percent of women and four percent of men over the age of thirty-five. Obesity is a significant contributing factor. In addition, patients are at greater risk of OSA with increasing age, due to loss of muscle mass, particularly within the muscles that would otherwise hold the respiration airway open.
Apnea can also occur during Cheyne-Stokes Respiration (CSR), which is an abnormal respiratory pattern often occurring in patients with CHF. CSR is characterized by alternating periods of hypopnea and hyperpnea (i.e. fast, deep breathing.) Briefly, CSR arises principally due to a time lag between blood CO2 levels sensed by the respiratory control nerve centers of the brain and the blood CO2 levels. With CHF, poor cardiac function results in poor blood flow to the brain such that respiratory control nerve centers respond to blood CO2 levels that are no longer properly representative of the overall blood CO2 levels in the body. Hence, the respiratory control nerve centers trigger an increase in the depth and frequency of breathing in an attempt to compensate for perceived high blood CO2 levels—although the blood CO2 levels have already dropped. By the time the respiratory control nerve centers detect the drop in blood CO2 levels and act to slow respiration, the blood CO2 levels have already increased. This cycle becomes increasingly unbalanced until respiration alternates between hypopnea and hyperpnea. The periods of hypopnea often become sufficiently severe that no breathing occurs between the periods of hyperpnea, i.e. periods of frank apnea occur between the periods of hyperpnea. The wildly fluctuating blood chemistry levels caused by alternating between hyperpnea and apnea/hypopnea can significantly exacerbate CHF and other medical conditions. When CHF is still mild, CSR usually occurs, if at all, only while the patient is sleeping. When it becomes more severe, CSR can occur while the patient is awake. Accordingly, CSR is one mechanism by which apnea can occur within patients who are awake. Apnea can also occur while awake due to neurological disorders or other factors. Hence, apnea is not limited to occurring only within sleeping patients.
Note that, in some of the literature, apnea arising due to CSR caused by CHF is categorized as a type of CSA (i.e. central sleep apnea), even though the apnea is not the result of a disorder of the central nervous system and even though it does necessarily occur only while the patient is asleep. Herein, however, CSA is only used to refer to apnea arising from a disorder of the central nervous system that occurs while a patient is asleep, as described above. Apnea/hypopnea arising because of CHF (such as via the mechanism of CSR respiration) is instead referred to herein as “CHF-induced apnea/hypopnea.”
In view of the significant adverse consequences of apnea/hypopnea, particularly insofar as patients with CHF are concerned, it is highly desirable to provide techniques for detecting individual episodes of the condition. A variety of techniques have been developed thus far. In particular, techniques have been developed that track changes in thoracic impedance as a means for tracking respiration so as to permit detection of apnea/hypopnea. In other words, the same impedance signal analyzed to detect heart failure/pulmonary edema can also be used to detect apnea. See, e.g., U.S. patent application Ser. No. 10/883,857, filed Jun. 30, 2004, entitled “System And Method For Real-Time Apnea/Hypopnea Detection Using An Implantable Medical System (A04P1057); U.S. patent application Ser. No. 10/844,023, filed May 11, 2004, entitled “System and Method for Providing Demand-Based Cheyne-Stokes Respiration Therapy Using an Implantable Medical Device” (A04P1042); and U.S. Pat. No. 6,449,509 to Park et al., entitled “Implantable Stimulation Device having Synchronous Sampling for a Respiration Sensor.” See, also, U.S. Pat. No. 5,974,340 to Kadhiresan, entitled “Apparatus and Method for Monitoring Respiratory Function in Heart Failure Patients to Determine Efficacy of Therapy.”
Problems, however, can arise when attempting to detect apnea/hypopnea via thoracic impedance in patients with pulmonary edema. The present inventor has noted that apnea detection via thoracic impedance is most reliable when the lungs are clear but is considerably less reliable when the lungs are filled with fluids, i.e. when the patient suffers from pulmonary edema. Hence, it is not always possible to reliably detect apnea using an impedance-based detection technique if the patient suffers from pulmonary edema. Accordingly, in addition to providing improved impedance-based techniques for detecting pulmonary edema as noted above, it is also desirable to provide techniques for determining when impedance-based reduced respiration detection techniques can reliably be used. It is to this end that other aspects of the invention are directed.